Egr­1 inhibits colon cancer cell proliferation, migration and invasion via regulating CDKL1 at the transcriptional level.

Colon cancer is one of the most common malignant tumors worldwide, and the molecular mechanisms involved in the oncogenesis and progression of colon cancer remain unclear. Early growth response 1 (Egr­1) is a transcription factor that is closely associated with several tumor processes; however, its role in colon cancer is unknown. The present study aimed to explore the function and mechanism of transcription factor Egr­1 in colon cancer progression. The association between Egr­1 expression and the survival of patients with colon cancer was analyzed. Transwell assay was used to measure the migration and invasion of colon cancer cells. Cell Counting Kit­8 assay was used to evaluate the cell proliferative ability. Reverse transcription­quantitative PCR and western blot assays were used to identify whether Egr­1 could regulate cyclin­dependent kinase­like 1 (CDKL1). Luciferase and chromatin immunoprecipitation assays were used to detect the mechanism by which Egr­1 regulated CDKL1. Based on The Cancer Genome Atlas database, it was found that low Egr­1 expression was associated with a poor prognosis in patients with colon cancer. Furthermore, overexpression of Egr­1 inhibited colon cancer cell proliferation, migration, and invasion, whereas knockdown of Egr­1 increased colon cancer cell proliferation, migration and invasion. Additionally, overexpression of Egr­1­induced cell proliferation, migration and invasion were reversed by overexpression of CDKL1. Furthermore, it was demonstrated that Egr­1 regulated CDKL1 expression at the transcriptional level. The present study illustrated the mechanism of Egr­1 regulating CDKL1, by which Egr­1 affected colon cancer cell proliferation, migration and invasion. The current findings suggested that Egr­1/CDKL1 may be a new promising target for the treatment of colon cancer.

Diagnostic ability of percutaneous core biopsy immediately after microwave ablation for lung ground-glass opacity.

OBJECTIVES: The objective of this study is to determine the diagnostic ability of percutaneous core biopsy immediately after microwave ablation (MWA) for lung ground-glass opacity (GGO). MATERIALS AND METHODS: Seventy-four patients with 74 lung GGOs were enrolled and treated with MWA. A percutaneous core needle biopsy was performed pre- and immediately post-MWA. All biopsy specimens were histologically examined by hematoxylin and eosin staining and immunostaining. Histologically, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA), and invasive adenocarcinoma (AC) were identified as positive, while chronic inflammation or normal lung tissue was identified as negative. RESULTS: The outcomes of pre-MWA histological diagnosis were AAH (n = 4), AIS (n = 16), MIA (n = 14), AC (n = 29), chronic inflammation (n = 2), and lung tissue (n = 9) with an 85.1% (63/74) positive diagnosis rate. The outcomes of the immediately post-MWA histological diagnosis were AAH (n = 5), AIS (n = 10), MIA (n = 11), AC (n = 29), chronic inflammation (n = 1), and lung tissue (n = 18) with a 74.3% (55/74) positive diagnosis rate. There was no significant difference in the positive diagnosis rate between the pre- and immediately post-MWA groups (P = 0.10). The outcomes of the combined diagnosis of pre- and immediately post-MWA were AAH (n = 4), AIS (n = 16), MIA (n = 16), AC (n = 31), chronic inflammation (n = 2), and lung tissue (n = 5) with a positive diagnosis rate of 90.5% (67/74), which was higher than that by pre-MWA biopsy (P < 0.05). The main complications were pneumothorax (n = 45, 60.8%), hemoptysis (n = 24, 32.4%), pleural effusion (n = 39, 52.7%), and pulmonary infection (n = 10, 13.5%). CONCLUSIONS: Immediately post-MWA core biopsy has promising efficacy for histological diagnosis of lung GGOs.